Table 1 Parkinson’s disease

Parkinson’s disease (PD) is a complex, progressive neurodegenerative condition affecting more than 1% of the population over 65 years of age. By the time clinical symptoms appear, around ~ 50% dopaminergic neurons in the substantia nigra pars compacta (SNpc), are lost. Most PD cases exhibit abnormal intracellular protein aggregates called Lewy bodies. These are composed largely of aggregated α-synuclein (α-syn). With the progression of the disease, the neurodegeneration in this region reaches 90%, while dopaminergic neuron loss in the dorsal tier may be as low as 25%, and many other brain regions are relatively unaffected [1]. The striatal selective neurodegeneration is clinically characterized by debilitating motor and non-motor features which cause severe disability [2]. About 10% of PD cases are monogenic forms, associated with highly penetrant gene mutations [3, 4]. However, the majority of PD cases are sporadic, with a complex etiology caused by an interplay of environmental and associated genetic risk factors. Over the last few years, large scale genome-wide association studies (GWAS) and meta-analyses have identified more than 90 loci of different frequency and penetrance associated with sporadic PD risk. Most of the loci confer a small PD risk individually, but have shown to possess a substantial cumulative risk [5,6,7,8,9].